User talk:Gmoney61

Copy and pasting

One of your edits appear to be copy and pasted from another source. We at Wikipedia usually require paraphrasing. If you own the copyright to this material please send permission for release under a CC BY SA license to permissions-en@wikimedia.org per WP:CONSENT. Doc James (talk · contribs · email) 03:41, 5 December 2014 (UTC)

Benactyzine

Doc James,

It was unfair of you to remove my post on the drug Benactyzine. My comment about its physical relaxant activities was not copied and pasted. They were words from my own mouth. I cited the source from which i gleaned the information from. I would sincerely hope you do not remove my posts from this point forward.

Gmoney61 — Preceding unsigned comment added by Gmoney61 (talk • contribs) 18:32, 5 December 2014 (UTC)

Let look at your edits.[1] You added:

"Certain muscarinic antagonists (e.g., atropine, aprophen, and benactyzine) are used as antidotes for the treatment of organophosphate poisoning. ... The interaction of aprophen and benactyzine, both aromatic esters of diethylaminoethanol, with nicotinic acetylcholine receptor (AChR) in BC3H-1 intact muscle cells and with receptor-enriched membranes of Torpedo californica /was examined/. Aprophen and benactyzine diminish the maximal carbamylcholine-elicited sodium influx into muscle cells without shifting Kact (carbamylcholine concentration eliciting 50% of the maximal 22Na+ influx). The concentration dependence for the inhibition of the initial rate of 22Na+ influx by aprophen and benactyzine occurs at lower concentrations (Kant = 3 and 50 microM, respectively) than those needed to inhibit the initial rate of [125I]-alpha-bungarotoxin binding to the agonist/antagonist sites of the AChR (Kp = 83 and 800 uM, respectively). The effective concentration for atropine inhibition of AChR response (Kant = 150 microM in BC3H-1 cells) is significantly higher than those obtained for aprophen and benactyzine. Both aprophen and benactyzine interact with the AChR in its desensitized state in BC3H-1 cells without further enhancing agonist affinity. Furthermore, these ligands do not alter the value of Kdes (equilibrium concentration of agonist which diminishes 50% of the maximal receptor response) in BC3H-1 muscle cells. The affinity of aprophen and benactyzine for the allosterically coupled noncompetitive inhibitor site of the AChR in Torpedo was determined using [3H]phencyclidine as a probe. Both compounds were found to preferentially associate with the high affinity (desensitized) state rather than the resting state of Torpedo AChR. There is a 14- to 23-fold increase in the affinity of aprophen and benactyzine for the AChR (KD = 0.7 and 28.0 uM in the desensitized state compared to 16.4 and 384 uM in the resting state, respectively). These data indicate that aprophen and benactyzine binding are allosterically regulated by the agonist sites of Torpedo AChR. Thus, aprophen and benactyzine are effective noncompetitive inhibitors of the AChR at concentrations of 1-50 uM, in either Torpedo or mammalian AChR. These concentrations correspond very well with the blood level of these drugs found in vivo to produce a therapeutic response against organophosphate poisoning"

ref says

"Certain muscarinic antagonists (e.g., atropine, aprophen, and benactyzine) are used as antidotes for the treatment of organophosphate poisoning. We have studied the interaction of aprophen and benactyzine, both aromatic esters of diethylaminoethanol, with nicotinic acetylcholine receptor (AChR) in BC3H-1 intact muscle cells and with receptor-enriched membranes of Torpedo californica. Aprophen and benactyzine diminish the maximal carbamylcholine-elicited sodium influx into muscle cells without shifting Kact (carbamylcholine concentration eliciting 50% of the maximal 22Na+ influx). The concentration dependence for the inhibition of the initial rate of 22Na+ influx by aprophen and benactyzine occurs at lower concentrations (Kant = 3 and 50 microM, respectively) than those needed to inhibit the initial rate of [125I]-alpha-bungarotoxin binding to the agonist/antagonist sites of the AChR (Kp = 83 and 800 microM, respectively). The effective concentration for atropine inhibition of AChR response (Kant = 150 microM in BC3H-1 cells) is significantly higher than those obtained for aprophen and benactyzine. Both aprophen and benactyzine interact with the AChR in its desensitized state in BC3H-1 cells without further enhancing agonist affinity. Furthermore, these ligands do not alter the value of Kdes (equilibrium concentration of agonist which diminishes 50% of the maximal receptor response) in BC3H-1 muscle cells. The affinity of aprophen and benactyzine for the allosterically coupled noncompetitive inhibitor site of the AChR in Torpedo was determined using [3H]phencyclidine as a probe. Both compounds were found to preferentially associate with the high affinity (desensitized) state rather than the resting state of Torpedo AChR. There is a 14- to 23-fold increase in the affinity of aprophen and benactyzine for the AChR (KD = 0.7 and 28.0 microM in the desensitized state compared to 16.4 and 384 microM in the resting state, respectively). These data indicate that aprophen and benactyzine binding are allosterically regulated by the agonist sites of Torpedo AChR. Thus, aprophen and benactyzine are effective noncompetitive inhibitors of the AChR at concentrations of 1-50 microM, in either Torpedo or mammalian AChR. These concentrations correspond very well with the blood level of these drugs found in vivo to produce a therapeutic response against organophosphate poisoning.

Basically you have copied and pasted the abstract of the article into Wikipedia [2] Doc James (talk · contribs · email) 18:50, 5 December 2014 (UTC)

Doc James,

This will not happen again. I apologize for copying and pasting the abstract from a primary source with its proper reference. This will not happen again. Can you please remove this block so i may add to this article

Sincerely,

Gmoney61

So there are two minimal expectations

1. You will always paraphrase
2. You will use high quality secondary sources like reviews per WP:MEDRS

If you agree we can unblock you. Doc James (talk · contribs · email) 22:13, 7 December 2014 (UTC)

I agree to these expectations

Gmoney61

Done. Doc James (talk · contribs · email) 00:26, 8 December 2014 (UTC)

This is not a high quality secondary source COADY, A; JEWESBURY, EC (3 March 1956). "A clinical trial of benactyzine hydrochloride (suavitil) as a physical relaxant". British medical journal. 1 (4965): 485–7. PMID 13293359.

It is a really old primary source.Doc James (talk · contribs · email) 05:44, 9 December 2014 (UTC)

There is no other sources about clinical information about Benactyzine. This is ridiculous. Primary sources are genuine sources. Please stop deleting my information. You are a doctor, you of all people should know that primary sources are legitimate. Please find someone else' page to hassle.

Sincerely,

Gmoney61

You prof really need to have a discussion with the core community of Wikipedia about the work he is having this class do. Would be happy to speak with them if you can put them in contact with me. Doc James (talk · contribs · email) 19:16, 9 December 2014 (UTC)

Doc James,

That wont be necessary. The work i am attempting to do is advancing the world's knowledge on this one drug by adding to this stub. I am bringing together the limited information available on this drug and paraphrasing it into wikipedia. There are a limited amount of secondary sources for this particular drug since it was removed from the market in the early 1970s. Therefore, i must use the limited sources i have to add to this stub. This information is scientifically sound and valid. By erasing this data, you are limiting this stub from becoming a legitimate wiki page.

Gmoney61

Yes this appears to be what all your classmates are doing. Thus you are all going to struggle. Secondary sources will be hard to find. Here is one here. Not the best project for you prof to assign. Doc James (talk · contribs · email) 19:44, 9 December 2014 (UTC)

This course focuses on drug translation. While clinical data is apart of it, there are other factors such as the commercial and regulatory aspects of the drugs. For this data, the documents from the FDA must be employed and patent information as well. If i am hearing you correctly, you do not want this type of information on this stub page? Why are you even reviewing benactyzine? This drug has been taken off the market for over 30 years now.

It was another editor that trimmed your content. FDA documents are good for some stuff. Patent applications, not so much. Doc James (talk · contribs · email) 20:44, 9 December 2014 (UTC)

Why are patent applications not sufficient? They clearly give particular commercial history of the drug in question.. User:Gmoney61

December 2014

You have been blocked from editing for a period of 7 days for copy and pasting. Once the block has expired, you are welcome to make useful contributions. If you think there are good reasons why you should be unblocked, you may appeal this block by adding the following text below this notice: {{unblock|reason=Your reason here ~~~~}}. However, you should read the guide to appealing blocks first.  Doc James (talk · contribs · email) 18:52, 5 December 2014 (UTC)

Basically you have copied and pasted in this edit [3]. You then denied that you did so.[4] It appears that we have different definitions of copy and pasting. Before you are allowed to edit again we will need an explanation for your edit. And a reassurance that it will not happen again. Best Doc James (talk · contribs · email) 18:56, 5 December 2014 (UTC)

note

Hi - i work on a bunch of health related articles and am interested in how drugs get discovered and developed. I am willing to help you craft some WP content that will "stick" if you are willing to follow instructions and don't bullshit me (you done a lot of that above.) Are you willing? Jytdog (talk) 22:29, 9 December 2014 (UTC)

Yes i am willing. This is part of a class i am taking which has requirements for what needs to go into our Wikipedia pages. Therefore, i am willing, but i am limited at the same time User talk:Gmoney61

fine. just here on your talk page, answer the following questions, and provide a link to the source where you found that information. At this point, any source will do. We have to start somewhere.

• what is the name of the company that brought the drug to market?

Merck Sharp & Dohme, Division Merck & Co ., Inc http://www.fda.gov/ohrms/dockets/98fr/FR1972_12_23_28437(6566).pdf

• in what year did they start to sell it?

1957 https://books.google.com/books?id=-5IABAAAQBAJ&pg=PA57&lpg=PA57&dq=merck+sharp+%26+dohme+Suavitil&source=bl&ots=o-__nOtxW-&sig=d_ZOTYTU4peJXm2rYHIbgEgct-w&hl=en&sa=X&ei=W3OIVO2kB8qnNq_KgqAD&ved=0CDIQ6AEwAw#v=twopage&q=suavitil&f=false

• in what year was it taken off the market?

Cant find anything yet — Preceding unsigned comment added by Gmoney61 (talk • contribs) 16:27, 10 December 2014 (UTC)

That will give us a place to start. i recently worked on another old drug like this.. it can be fun detective work. Jytdog (talk) 22:58, 9 December 2014 (UTC)

nicely done! actually your first reference there, provides the date. it is 1972. OK, that first reference is from the Federal Register and is about a DESI case. It also mentions an earlier posting in the Federal Register: "In a notice (DESI 6566) published in the FEDERAL REGISTER of June 25, 1970 (35 F.R. 10394)..." A question and a request:

question: Do you know what a "DESI" is? if not, please read Drug Efficacy Study Implementation and let me know if you have any questions...

Would you please find that earlier federal register article (note, the internet archive has all of them) and provide a link? Jytdog (talk) 17:20, 10 December 2014 (UTC)

Okay i found it, but i had to access i through my university and i saved the pdf on my desktop. How do i upload it to here? — Preceding unsigned comment added by Gmoney61 (talk • contribs) 19:17, 10 December 2014‎(UTC)

Would you please sign your posts by putting four tildas after them? (Like this: ~~~~. The wikipedia software automatically changes that into your username and date.)

You don't need to mess around with uploading it - there doesn't have to be links to everything - just a reference that someone else can track down, like you did. But would you please email it to me? My email is my username at gmail. Thanks Jytdog (talk) 19:21, 10 December 2014 (UTC)

Do you understand the DESI thing, or not? Jytdog (talk) 19:21, 10 December 2014 (UTC)

Okay, and i do understand the DESI thing. The U.S. govenrment implemented the program to review and evaluate the effectiveness of the drugs on the market as a way to regulate what drugs should and shouldnt be allowed to adminstered.....--Gmoney61 (talk) 19:31, 10 December 2014 (UTC)

ok that is close but no cigar. FDA law has evolved. (tbe following is a rough history) The very first versions of the law, requried only that food, drugs, and cosmetics were "pure" - that they were not "adulterated" with anything known to be harmful. The next big change was the one in the early 1960s, that said that no drug could be on the market unless it was effective (it is not about whether a doctor prescribe it, or someone could "administer" it -- it is whether the drug can be on market at all). The next big change came in the early 1970s, which said that new drugs also had to be proven safe (this happened after the thalidomide scandal). Nowadays, companies have to show that their drugs are safe and effective before the FDA will approve them.

That big change in the 1960s gave the FDA a huge headache, since there were hundreds of drugs already on the market. What about them? The deal that was set up, was that the National Academy of Sciences (a disinterested body) got paid to review the scientific literature on each drug, and make a judgement if it worked, or maybe worked or did not work. That report is the DESI. The NAS sent that report on each drug to the FDA, which in turn had to send it to the company selling the drug. If the DESI found the drug effective, the FDA would tell the company they could keep marketing it. If the DESI found the drug not to be effective, the FDA would tell the company to stop selling it. If the DESI found that the drug maybe worked, the FDA would tell the company that it had to either submit new data showing that the drug is effective, or withdraw the drug from the market. If the company did nothing, the FDA would follow up with a letter saying that the drug had to be taken off the market. And the FDA had to report all this in the Federal Register. That is the bigger story here.

The Federal Register issue that you emailed to me, is the report of the first action; the FDA had received the DESI and informed the companies of what they had to do. The Federal Register that you linked to above, is the report of the second action.

Does that all make sense? am looking for a yes/no, and if no, a question about what is unclear... Jytdog (talk) 19:56, 10 December 2014 (UTC)

Yes that all makes sense. The FDA pulled benactyzine off the market because Merck and Co couldnt prove its effectiviness and safety. Okay, so where do we go from here? I need to add to that drug's page before my class tonight --Gmoney61 (talk) 20:04, 10 December 2014 (UTC)

That is not right. please slow down and read again. i need to know if you understand the big picture or not. Jytdog (talk) 20:05, 10 December 2014 (UTC)

Okay, i get the big picture now. I see what the FDA was trying to do - Essentially implent these new laws and for the drugs that were already on the market - check them out...--Gmoney61 (talk) 20:09, 10 December 2014 (UTC)

that's better, yes. ok, with all this in hand, you will be able to draft some wikipedia content. you can do some copy/pasting from content I created here - the research I recently did that led me into this strange time: Stanozolol#History (note - this is just in the history section of that article for now because I haven't time to rework that whole article, which the bodybuilding idiots have turned into something bad...). Please post your draft below. Jytdog (talk) 20:17, 10 December 2014 (UTC)

draft

In 1957, benactyzine was brought to market in the US by Merck Sharp & Dohme (a of division of Merck & Co) under the tradename "Suavitil".WRONG REF. FLESH OUT REF IN ANY CASE

In 1962, the Kefauver Harris Amendment was passed, amending the Federal Food, Drug, and Cosmetic Act to require drug manufacturers to provide proof of the effectiveness of their drugs before approval. The FDA implemented its Drug Efficacy Study Implementation (DESI) program to study and regulate drugs, including stanozolol, that had been introduced prior to the amendment. The DESI program was intended to classify all pre-1962 drugs that were already on the market as either effective, ineffective, or needing further study. The FDA enlisted the National Research Council of the National Academy of Sciences to evaluate publications on relevant drugs under the DESI program.

In 1970, the DESI review for benactyzine was completed and the NAS/NRC found that benactyzine was _____________ (pfill in from ref), and the FDA told Merck Sharp & Dohme ______________ (you didn't read the reference to see what it actually says. I said NO BULLSHIT) Two years later, _________________________________. ref name=FedReg1970WRONG REFERENCE AND PLEASE FILL IN THE INFORMATION FROM WHAT THE REFERENCE ACTUALLY SAYS

so.. that was disappointing. i revised it. I am done trying to help you. if you try to insert crap content into the article it will be reverted. Jytdog (talk) 22:11, 10 December 2014 (UTC)

Speedy deletion nomination of File:Federal Register Notice, June 25, 1970.pdf

A tag has been placed on File:Federal Register Notice, June 25, 1970.pdf requesting that it be speedily deleted from Wikipedia. This has been done under section F10 of the criteria for speedy deletion, because it is a file that is not an image, sound file or video clip (e.g. a Word document or PDF file) that has no encyclopedic use.

If you think this page should not be deleted for this reason, you may contest the nomination by visiting the page and clicking the button labelled "Contest this speedy deletion". This will give you the opportunity to explain why you believe the page should not be deleted. However, be aware that once a page is tagged for speedy deletion, it may be deleted without delay. Please do not remove the speedy deletion tag from the page yourself, but do not hesitate to add information in line with Wikipedia's policies and guidelines. Pkbwcgs (talk) 09:48, 22 August 2018 (UTC)